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Molecular basis of multiple resistance to ACCase‐inhibiting and ALS‐inhibiting herbicides in Lolium rigidum
Author(s) -
TAN MK,
PRESTON C,
WANG GX
Publication year - 2007
Publication title -
weed research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.693
H-Index - 74
eISSN - 1365-3180
pISSN - 0043-1737
DOI - 10.1111/j.1365-3180.2007.00591.x
Subject(s) - lolium rigidum , acetolactate synthase , biology , genetics , weed , mutant , gene , sulfonylurea , weed control , outcrossing , cross resistance , herbicide resistance , botany , agronomy , microbiology and biotechnology , pollen , insulin
Summary Herbicide resistance in Lolium rigidum is widespread across much of the agricultural land in Australia. As the incidence of herbicide resistance has increased, so has the incidence of multiple herbicide resistance. This reduces the herbicide options available for control of this weed. This study reports on the successful amplification and sequencing of the acetolactate synthase (ALS) gene of L. rigidum using primers designed from sequence information of related taxa. This enables, for the first time, the successful determination of a mutation in the ALS gene of this species that provides resistance to ALS‐inhibiting herbicides. This mutation causes amino acid substitution at Trp574 (numbering standardised to Arabidopsis thaliana ) to Leu which had been reported to confer a high level of resistance against all classes of ALS inhibitor herbicides. In addition, multiple resistance to ALS‐inhibiting and acetyl‐coenzyme A carboxylase‐inhibiting herbicides is acquired through the independent accumulation of mutant alleles for the target sites. This may thus explain some of the irregular, mosaic resistance patterns that occur in this predominantly outcrossing species.